The present invention is directed to a medical product and operation procedure which can be used to correct vision loss or even complete blindness caused by certain retinal diseases. A variety of retinal diseases, for example, cause vision loss or blindness by destruction of the choroid, choriocapillaris, and the outer retinal layers. The outer layers include Bruch's membrane and retinal pigment epithelium, the loss of which results in degeneration of the inner retinal photoreceptor layer. These diseases, however, often spare much of the remaining inner retinal layers of the outer nuclear, outer plexiform, inner nuclear, inner plexiform, ganglion cell and nerve fiber layers.
The current invention involves the use of an electronic device, a photosensitive array, that is capable of mimicking the signals that would otherwise be produced by the damaged inner retinal photoreceptor layer. When the device is implanted between the inner and outer retinal layers, it will stimulate the inner layer to provide significantly useful formed vision to a patient in a manner never before available.
Prior attempts have been made to produce vision by stimulating various portions of the retina. One such attempt involved an externally powered but internally located photosensitive array device with its photoactive surface and electrode surface on opposite sides. The device was to stimulate the nerve fiber layer via direct placement on this layer from the vitreous body side. The success of this device is unlikely due to it having to duplicate the complex frequency modulate neural signals of the nerve fiber layer. Furthermore, the nerve fiber layer runs in a general radial course with many layers of overlapping fibers from different portions of the retina making selection of the appropriate nerve fiber to stimulate extremely difficult if not impossible. The production of useful formed visual imagery is therefore highly unlikely. No device of this type has been known to have been constructed that produced any type of formed image.
Another prior device involved a unit consisting of a supporting base onto which a photo-sensitive material such as selenium is coated. This device was to have been inserted through an external scleral incision made at the posterior pole resting between the sclera and choroid or between the choroid and retina. Light stimulation would then cause a potential to develop on the photosensitive surface causing ions to be produced which would then theoretically migrate into the retina causing stimulation. However, having no discrete surface structure to restrict the directional flow of charges, lateral migration and diffusion of charges would be allowed thereby preventing any resolution capability. Placement of this device between the sclera and choroid would also virtually block the discrete migration of ions to the photoreceptor and inner retinal layers due to the presence of the choroid, choriocapillaris, Bruch's membrane and the retinal pigment epithelial layer. Placement of the device between the choroid and the retina would still interpose Bruch's membrane and the retinal pigment epithelial layer in the pathway of discrete ion migration. Also, as this device would have had to be inserted into or through the highly vascular choroid of the posterior pole, severe subchoroidal, intraretinal and or intraorbital hemorrhage would likely have resulted along with disruption of blood flow to the posterior pole. One such device was apparently constructed and implanted into a patient's eye resulting in reported light perception but no formed imagery.